The compatibility of a nucleopolyhedrosis virus control with resistance management for Bacillus thuringiensis: Co-infection and cross-resistance studies with the diamondback moth, Plutella xylostella

2006 ◽  
Vol 93 (2) ◽  
pp. 114-120 ◽  
Author(s):  
B. Raymond ◽  
A.H. Sayyed ◽  
D.J. Wright
2001 ◽  
Vol 67 (7) ◽  
pp. 3216-3219 ◽  
Author(s):  
Yong-Biao Liu ◽  
Bruce E. Tabashnik ◽  
Susan K. Meyer ◽  
Neil Crickmore

ABSTRACT We tested toxins of Bacillus thuringiensis against larvae from susceptible, Cry1C-resistant, and Cry1A-resistant strains of diamondback moth (Plutella xylostella). The Cry1C-resistant strain, which was derived from a field population that had evolved resistance to B. thuringiensis subsp.kurstaki and B. thuringiensis subsp.aizawai, was selected repeatedly with Cry1C in the laboratory. The Cry1C-resistant strain had strong cross-resistance to Cry1Ab, Cry1Ac, and Cry1F, low to moderate cross-resistance to Cry1Aa and Cry9Ca, and no cross-resistance to Cry1Bb, Cry1Ja, and Cry2A. Resistance to Cry1C declined when selection was relaxed. Together with previously reported data, the new data on the cross-resistance of a Cry1C-resistant strain reported here suggest that resistance to Cry1A and Cry1C toxins confers little or no cross-resistance to Cry1Bb, Cry2Aa, or Cry9Ca. Therefore, these toxins might be useful in rotations or combinations with Cry1A and Cry1C toxins. Cry9Ca was much more potent than Cry1Bb or Cry2Aa and thus might be especially useful against diamondback moth.


Author(s):  
Jing Wang ◽  
Xiaobin Zheng ◽  
Jiangjiang Yuan ◽  
Shuaiyu Wang ◽  
Baoyun Xu ◽  
...  

Abstract The diamondback moth, Plutella xylostella L., is a worldwide crop pest that is difficult to control because of its ability to develop resistance to many insecticides. To provide a reference for resistance management of P. xylostella in China, the present study used a leaf-dip bioassay to monitor the resistance of P. xylostella to nine insecticides in eight regions of China. The results showed that P. xylostella had developed a high level of resistance to beta-cypermethrin (resistance ratio [RR] > 112), and moderate (RR < 40) to high levels of resistance to indoxacarb, abamectin, and chlorfluazuron. For chlorantraniliprole, RRs > 100 were found in Midu (Yunnan Province) and Jinghai (Tianjin). In most regions, the resistance to spinetoram and chlorfenapyr and Bacillus thuringiensis (Bt) was low. No resistance was detected to diafenthiuron. Overall, P. xylostella resistance to insecticides was higher in Midu than in other regions. The data in this study should help guide the selection of insecticides for management of P. xylostella in China.


2000 ◽  
Vol 66 (4) ◽  
pp. 1509-1516 ◽  
Author(s):  
Ali H. Sayyed ◽  
Robert Haward ◽  
Salvador Herrero ◽  
Juan Ferré ◽  
Denis J. Wright

ABSTRACT Four subpopulations of a Plutella xylostella (L.) strain from Malaysia (F4 to F8) were selected with Bacillus thuringiensis subsp.kurstaki HD-1, Bacillus thuringiensis subsp. aizawai, Cry1Ab, and Cry1Ac, respectively, while a fifth subpopulation was left as unselected (UNSEL-MEL). Bioassays at F9 found that selection with Cry1Ac, Cry1Ab, B. thuringiensissubsp. kurstaki, and B. thuringiensis subsp. aizawai gave resistance ratios of >95, 10, 7, and 3, respectively, compared with UNSEL-MEL (>10,500, 500, >100, and 26, respectively, compared with a susceptible population, ROTH). Resistance to Cry1Ac, Cry1Ab, B. thuringiensis subsp. kurstaki, andB. thuringiensis subsp. aizawai in UNSEL-MEL declined significantly by F9. The Cry1Ac-selected population showed very little cross-resistance to Cry1Ab, B. thuringiensis subsp. kurstaki, andB. thuringiensis subsp. aizawai(5-, 1-, and 4-fold compared with UNSEL-MEL), whereas the Cry1Ab-,B. thuringiensis subsp. kurstaki-, and B. thuringiensis subsp.aizawai-selected populations showed high cross-resistance to Cry1Ac (60-, 100-, and 70-fold). The Cry1Ac-selected population was reselected (F9 to F13) to give a resistance ratio of >2,400 compared with UNSEL-MEL. Binding studies with125I-labeled Cry1Ab and Cry1Ac revealed complete lack of binding to brush border membrane vesicles prepared from Cry1Ac-selected larvae (F15). Binding was also reduced, although less drastically, in the revertant population, which indicates that a modification in the common binding site of these two toxins was involved in the resistance mechanism in the original population. Reciprocal genetic crosses between Cry1Ac-reselected and ROTH insects indicated that resistance was autosomal and showed incomplete dominance. At the highest dose of Cry1Ac tested, resistance was recessive while at the lowest dose it was almost completely dominant. The F2 progeny from a backcross of F1 progeny with ROTH was tested with a concentration of Cry1Ac which would kill 100% of ROTH moths. Eight of the 12 families tested had 60 to 90% mortality, which indicated that more than one allele on separate loci was responsible for resistance to Cry1Ac.


2008 ◽  
Vol 98 (2) ◽  
pp. 145-157 ◽  
Author(s):  
N.M. Endersby ◽  
P.M. Ridland ◽  
A.A. Hoffmann

AbstractWhen strong directional selection acts on a trait, the spatial distribution of phenotypes may reflect effects of selection, as well as the spread of favoured genotypes by gene flow. Here we investigate the relative impact of these factors by assessing resistance to synthetic pyrethroids in a 12-year study of diamondback moth, Plutella xylostella, from southern Australia. We estimated resistance levels in populations from brassicaceous weeds, canola, forage crops and vegetables. Differences in resistance among local populations sampled repeatedly were stable over several years. Levels were lowest in samples from weeds and highest in vegetables. Resistance in canola samples increased over time as insecticide use increased. There was no evidence that selection in one area influenced resistance in adjacent areas. Microsatellite variation from 13 populations showed a low level of genetic variation among populations, with an AMOVA indicating that population only accounted for 0.25% of the molecular variation. This compared to an estimate of 13.8% of variation accounted for by the resistance trait. Results suggest that local selection rather than gene flow of resistance alleles dictated variation in resistance across populations. Therefore, regional resistance management strategies may not limit resistance evolution.


1997 ◽  
Vol 87 (5) ◽  
pp. 481-486 ◽  
Author(s):  
M. Iqbal ◽  
D.J. Wright

AbstractThe efficacy of abamectin (AgrimecR) and teflubenzuron (NomoltR) was assessed by leaf-dip bioassay against larvae of the diamondback moth, Plutella xylostella Linnaeus from a population (SERD3) collected originally in lowland Malaysia in December 1994. Evidence for resistance to both abamectin and teflubenzuron was found in the F7 generation (LC50 ratio of 60 and 24 respectively compared with a laboratory, insecticide-susceptible strain). Selection of sub-populations of SERD3 (F7–F9) with abamectin and teflubenzuron increased the LC50 ratio to 220 and 360 respectively and estimates of realized heritability [h2] were high (c. 0.8 and 0.9) for both compounds. There was no cross-resistance between these compounds in the abamectin and teflubenzuron-selected sub-populations but some indication of negatively-correlated resistance. Topical application of the synergists piperonyl butoxide, S,S,S-tributylphosphorotrithioate and maleic acid diethyl ester to the laboratory strain had no significant effect on the toxicity of abamectin or teflubenzuron in subsequent leaf-dip assays. In contrast, pre-treatment with piperonyl butoxide and S,S,S-tributylphosphorotrithioate significantly increased the toxicity of abamectin (c. 4- and 3-fold) and teflubenzuron (c. 7- and 19-fold) in the abamectin and teflubenzuron-selected sub-populations of SERD3, suggesting that microsomal monoxygenases and/or esterases may be involved in resistance. Pre-treatment with maleic acid diethyl ester only increased the toxicity of abamectin by c. 2-fold and had no significant effect on the toxicity of teflubenzuron, providing limited evidence for the involvement of glutathione-S-transferases in resistance to the former compound alone.


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